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Involvement of Oxidative Stress in Formaldehyde-induced Apoptosis in Cultured Lung Macrophage Cells

폐 대식세포주에서 포름알데히드에 의한 세포 사멸 효과에 대한 산화성 스트레스 관련성

  • Park, Soo-Hyun (Bio-therapy Human Resources Center, Animal Medical Center, Department of Veterinary Physiology, College of Veterinary Medicine, Chonnam National University)
  • 박수현 (전남대학교 수의과대학 바이오치료 산업인력 양성팀, 동물의학 연구소)
  • Published : 2009.09.30

Abstract

Formaldehyde (FA) is an important irritant compound in pesticide to induce asthma and allergy in respiratory system. Alveolar macrophage is also an pivotal cell in the immune response of respiratory system. However, the effect of FA in macrophage cell viability has not been elucidated. Thus, this study was conducted to investigate the effect of FA on apoptosis in Raw 264.7 cells, alveolar macrophage cell line. In this study, FA decreased cell viability of lung alveolar macrophage cells in a dose-dependent manner (>$100{\mu}M$). FA-induced decrease of cell viability was blocked by the treatment of antioxidants (vitamin C, NAC, and catalase). Indeed, FA induced lipid peroxide formation in Raw 264.7 cells. FA decreased Bcl-2 expression but increased Bax expression in lung alveloar macrophage cells. In addition, FA also increased the cleaved form of caspase-3. In conclusion, FA induced apoptosis via oxidative stress in cultured Raw 264.7 cells.

포름알데히드는 농약 노출 시에 나타나는 중요한 물질로 천식 및 알러지등의 호흡 질환을 일으키는 물질로 알려져 있으며, 폐에서 대식세포는 면역 반응에 있어서 방어 기능을 담당하는 세포로 알려져 있다. 그러나 대식세포에서 포름알데히드에 대한 효과는 알려져 있지 않고 있어서 대식 세포주인 Raw 264.7 세포를 이용하여 실험하였다. 실험 결과 포름알데히드는 세포 생존율을 감소 시켰으며, 이러한 반응은 항산화제인 vitamin C, NAC, 및 catalase 처리 시 차단되었다. 실제로 포름알데히드 처리시 산화성 스트레스 지표인 lipid peroxide 형성이 증가하였으며 이들 반응 역시 항산화제들에 의해 차단되었다. 한편 포름알데히드 처리시 세포 사멸 촉진 단백질인 Bax 발현은 증가하였으며 세포 사멸 억제 단백질인 Bcl-2의 발현은 억제되었으며 이러한 반응은 항산화제 처리시 차단되었다. 세포사멸 실행 단백질인 casapse-3의 활성형 역시 증가하였으며, 항산화제 처리시 차단되었다. 결론적으로 포름알데히드는 폐 대식세포에서 산화성 스트레스 증가를 통해 세포 사멸을 일으키는 것으로 나타났다.

Keywords

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